Cholinergic anti-inflammatory pathway: Difference between revisions
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The '''Cholinergic Anti-inflammatory Pathway''' regulates the innate immune response {{[[Innate immunity]]}} to injury, pathogens, and tissue ischemia. It is the efferent, or motor arm of the |
The '''Cholinergic Anti-inflammatory Pathway''' regulates the innate immune response {{[[Innate immunity]]}} to injury, pathogens, and tissue ischemia. It is the efferent, or motor arm of the [[Inflammatory Reflex]], the neural circuit that responds to and regulates the inflammatory response.<ref>{{cite doi|10.1038/nature0132}}</ref> |
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== Regulating the Immune Response == |
== Regulating the Immune Response == |
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Tumor Necrosis Factor ([[TNF]]) (and other [[cytokines]] are produced by cells of the innate immune system during local injury and infection. These contribute to initiating a cascade of mediator release, and recruiting inflammatory cells to the site of infection to contain infection, referred to as "[[innate immunity]].". TNF amplifies and prolongs the inflammatory response by activating other cells to release [[interleukin-1]] (IL-1), [[high mobility group]] B1 ([[HMGB1]]) and other cytokines.<ref>{{cite doi|10.1177/09680519010070041401}}</ref> These inflammatory cytokine responses confer protective advantages to the host at the site of [[Infection|bacterial infection]]. A “beneficial” inflammatory response is limited, resolves in 48-72 hours, and does not spread systemically. The cholinergic anti-inflammatory pathway provides a braking effect on the innate immune response which protects the body against the damage that can occur if a localized inflammatory response spreads beyond the local tissues, which results in toxicity or damage to the [[kidney]], [[liver]], [[lungs]], and other organs. |
Tumor Necrosis Factor ([[TNF]]) (and other [[cytokines]]) are produced by cells of the innate immune system during local injury and infection. These contribute to initiating a cascade of mediator release, and recruiting inflammatory cells to the site of infection to contain infection, referred to as "[[innate immunity]].". TNF amplifies and prolongs the inflammatory response by activating other cells to release [[interleukin-1]] (IL-1), [[high mobility group]] B1 ([[HMGB1]]) and other cytokines.<ref>{{cite doi|10.1177/09680519010070041401}}</ref> These inflammatory cytokine responses confer protective advantages to the host at the site of [[Infection|bacterial infection]]. A “beneficial” inflammatory response is limited, resolves in 48-72 hours, and does not spread systemically. The cholinergic anti-inflammatory pathway provides a braking effect on the innate immune response which protects the body against the damage that can occur if a localized inflammatory response spreads beyond the local tissues, which results in toxicity or damage to the [[kidney]], [[liver]], [[lungs]], and other organs. |
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== Neurophysiological and Immunological Mechanism == |
== Neurophysiological and Immunological Mechanism == |
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Revision as of 20:51, 30 December 2010
The Cholinergic Anti-inflammatory Pathway regulates the innate immune response {{Innate immunity}} to injury, pathogens, and tissue ischemia. It is the efferent, or motor arm of the Inflammatory Reflex, the neural circuit that responds to and regulates the inflammatory response.[1]
Regulating the Immune Response
Tumor Necrosis Factor (TNF) (and other cytokines) are produced by cells of the innate immune system during local injury and infection. These contribute to initiating a cascade of mediator release, and recruiting inflammatory cells to the site of infection to contain infection, referred to as "innate immunity.". TNF amplifies and prolongs the inflammatory response by activating other cells to release interleukin-1 (IL-1), high mobility group B1 (HMGB1) and other cytokines.[2] These inflammatory cytokine responses confer protective advantages to the host at the site of bacterial infection. A “beneficial” inflammatory response is limited, resolves in 48-72 hours, and does not spread systemically. The cholinergic anti-inflammatory pathway provides a braking effect on the innate immune response which protects the body against the damage that can occur if a localized inflammatory response spreads beyond the local tissues, which results in toxicity or damage to the kidney, liver, lungs, and other organs.
Neurophysiological and Immunological Mechanism
The Vagus Nerve is the tenth cranial nerve. It regulates heart rate, bronchoconstriction, digestion, and the innate immune response. The vagus nerve innervates the celiac ganglion, the site of origin of the splenic nerve. Stimulation of the efferent vagus nerve slows heart rate, induces gastric motility, and inhibits TNF production in spleen. Stimulation of the efferent pathway of the vagus nerve releases acetylcholine, the neurostransmitter which interacts with the α7 subunit of the nicotinic AChR (α7 nAChR). nAChR is expressed on the cell membrane of macrophages and other cytokine secreting cells. Binding of acetylcholine to nAChR activates intracellular signal transduction which inhibits release of pro-inflammatory cytokines. Ligand receptor signaling does suppress production of anti-inflammatory cytokines (IL-10)[3].
References
- ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1038/nature0132, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with
|doi=10.1038/nature0132instead. - ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1177/09680519010070041401, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with
|doi=10.1177/09680519010070041401instead. - ^ Chatterjee PK, Al-Abed Y, Sherry B, Metz CN (2009). "Cholinergic agonists regulate JAK2/STAT3 signaling to suppress endothelial cell activation". Am. J. Physiol., Cell Physiol. 297 (5): C1294–306. doi:10.1152/ajpcell.00160.2009. PMC 2777398. PMID 19741199.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link)Nicolussi EM, Huck S, Lassmann H, Bradl M (2009). "The cholinergic anti-inflammatory system limits T cell infiltration into the neurodegenerative CNS, but cannot counteract complex CNS inflammation". Neurobiol. Dis. 35 (1): 24–31. doi:10.1016/j.nbd.2009.03.010. PMID 19344760.{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link)Johnston GR, Webster NR (2009). "Cytokines and the immunomodulatory function of the vagus nerve". Br J Anaesth. 102 (4): 453–62. doi:10.1093/bja/aep037. PMID 19258380.{{cite journal}}: Unknown parameter|month=ignored (help)